炎症相关因素对骨质疏松症影响研究进展
Research advances in the impact of inflammation-related factors on osteoporosis
  
DOI:10.3969/j.issn.1006-7108.2026.02.011
中文关键词:  骨质疏松症  炎症  免疫细胞  NLRP3炎性小体
英文关键词:osteoporosis  inflammation  immune cells  NLRP3 inflammasome
基金项目:国家自然科学基金面上项目(82305275)
作者单位
王时誉1 孙广江2* 1.辽宁中医药大学,辽宁 沈阳 110847 2.辽宁中医药大学附属医院,辽宁 沈阳 110000 
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中文摘要:
      骨质疏松症(osteoporosis,OP)是一种常见的骨代谢异常疾病,全球数以亿计人患有此病,特别是老年患者,此病患病率常年居高不下,是影响老年患者生存和健康的巨大威胁。炎症在骨质疏松症的发病机制中发挥着关键作用,尤其是白细胞类群、抗原呈递细胞和NLRP3炎性小体的参与。慢性炎症通过免疫细胞(如Th17/Treg失衡、M1/M2型巨噬细胞极化)及其分泌的炎性细胞因子(如TNF-α、IL-6、IL-17等)影响骨代谢,形成“破骨增强-成骨抑制”的恶性循环。炎性细胞因子通过RANKL/OPG、NF-κB、Wnt等信号通路交互作用,进一步促进骨质流失。NLRP3炎性小体的激活不仅加剧炎症反应,还通过抑制成骨分化和促进破骨生成加速骨吸收。本综述从白细胞类群、抗原呈递细胞类群和NLRP3炎性小体三个与炎症密切相关的维度出发,系统整合当前炎症调控骨代谢的分子机制及治疗策略,以期为后续治疗研究提供思路。
英文摘要:
      Osteoporosis (OP) is a common metabolic bone disorder that affects hundreds of millions of people worldwide, particularly among elderly individuals. The persistently high prevalence of this disease poses a significant threat to the survival and health of elderly patients. Inflammation plays a crucial role in the pathogenesis of osteoporosis, particularly through the involvement of leukocyte subsets, antigen-presenting cells, and the NLRP3 inflammasome. Chronic inflammation influences bone metabolism through immune cells (such as Th17/Treg imbalance and M1/M2 macrophage polarization) and their secreted inflammatory cytokines (such as TNF-α, IL-6, and IL-17), leading to a vicious cycle of enhanced bone resorption and inhibited bone formation. Inflammatory cytokines interact through signaling pathways such as RANKL/OPG, NF-κB, and Wnt, further exacerbating bone loss. Activation of NLRP3 inflammasome not only intensifies the inflammatory response but also accelerates bone resorption by inhibiting osteogenic differentiation and promoting osteoclastogenesis. This review systematically integrates current molecular mechanisms and therapeutic strategies related to inflammation-regulated bone metabolism from three inflammation-associated perspectives: leukocyte subsets, antigen-presenting cells, and the NLRP3 inflammasome, aiming to provide insights for future therapeutic research.
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